The long-term goal is to understand the cellular and molecular mechanisms of vibration syndrome in order to define countermeasures to prevent injury and promote the safer use of power tools. A new animal model of vibration injury, employing the rat's tail, is introduced for studying the primary effects of short- and long-term vibration on specific tissues. The general hypothesis is that vibration injury results from combined neural and vascular damage. Specific hypotheses are: 1. Vibration injury begins with disruption of the schwann cells and cytoskeleton of large myelinated nerve fibers which degrades general sensation and skeletal muscle function. Small nerve fibers, associated with pain and vasomotor regulation, are initially spared. 2. Vibration stimulates vasospasm of arteries. This induces hypertrophy and hyperplasia of smooth muscle cells and intimal matrix reorganization, which culminates in chronic vessel occlusion and ischemia. 3. Vibration damage disrupts axoplasmic transport in large neurons. This exacerbates injury by blocking trophic interactions between the neurons and end organs. Detection of the earliest cell types responding to vibration will be accomplished by immunostaining with cell type specific markers, for immediate early gene protein (phosphorylated c-jun) expression and for proliferation by bromodeoxyuridine incorporation. Electron microscopy is employed to resolve primary ultrastructural damage. Functional changes will be assessed my measurements of tail skin temperature, blood flow, reflex withdrawal to noxious and touch stimulation, compound nerve action potential recording, and retrograde labeling of neurons. 4. Tissue specific sensitivity to injury is frequency (30, 60 and 120 Hz) on nerve, artery and skeletal muscle tissues will be compared. These studies will further the understanding of the pathophysiology of vibration disease and provide insight into novel treatment strategies.